Parallel clinical and animal studies of the pathophysiologic mechanisms of ocular hypotony in eyes with ciliochoroidal detachment, retinal detachment, or cyclodialysis will be performed. A model of experimental hypotony in rhesus monkeys, secondary to experimentally-produced ciliochoroidal or retinal detachment, has been developed. The rate of aqueous formation and the rates of conventional (via Schlemm's canal) and uveoscleral outflow will be measured in the animal models to determine the cause of hypotony. The importance of coexistent iridocyclitis as a basic cause of hypotony in these eyes, suggested by pilot studies, will be further evaluated. Preliminary experiments have identified a drug combination capable of reversing experimentally-induced hypotony. This effect is presumably due to stimulation of the aqueous formation rate. To test this, the aqueous formation rate will be measured before and after treatment with these drugs in eyes with experimental hypotony. Eyes of patients with hypotony, secondary to ciliochoroidal detachment, retinal detachment, or cyclodialysis will be studied. Aqueous flow will be measured with fluorophotometry before and after treatment or abatement of the hypotony. Episcleral venous pressure will also be measured and will be compared to the intraocular pressure to determine if a pressure head for conventional outflow exists. The degree of iridocyclitis in eyes with hypotony will be compared to the rate of aqueous humor formation to determine if a correlation exists. A group of uncomplicated cases following intraocular surgery will be studied to determine if reduced aqueous humor formation is a normal sequel to intraocular surgery, or if it is present only in eyes with marked hypotony. A small number of eyes with hypotony due to chronic iridocyclitis will be studied, as above, for comparative purposes.